A5050126209- Coagulation, Bradykinin, Polyphosphates, and Angioedema
- Urticaria and Related Conditions
- Hemophilia Treatment and Research
- Drug-Induced Adverse Reactions
- Autoimmune Bullous Skin Diseases
- Contact Dermatitis and Allergies
- Allergic Rhinitis and Sensitization
- Dermatology and Skin Diseases
- Food Allergy and Anaphylaxis Research
- Asthma and respiratory diseases
- Vitamin K Research Studies
- Mast cells and histamine
- Pharmaceutical studies and practices
- Chronic Myeloid Leukemia Treatments
- Pediatric health and respiratory diseases
- Metabolism and Genetic Disorders
- Enzyme function and inhibition
- Immunodeficiency and Autoimmune Disorders
- Peptidase Inhibition and Analysis
- Pharmaceutical industry and healthcare
- Occupational exposure and asthma
- Child Nutrition and Feeding Issues
- Heparin-Induced Thrombocytopenia and Thrombosis
- Pneumocystis jirovecii pneumonia detection and treatment
- Microscopic Colitis
ENT and Allergy
2011-2025
Structural Analytics (United States)
2023
Phelps Hospital
2023
Winthrop-University Hospital
2011-2020
Scientific and clinical progress together with the development of effective novel therapeutic options has engendered multiple important changes in diagnosis management hereditary angioedema (HAE). We now update extend 2013 United States Hereditary Angioedema Association Medical Advisory Board guidelines for treatment HAE. The are based on a comprehensive literature review recommendations indicating both strength our recommendation quality underlying evidence. Guidelines provided regarding...
Current treatments for long-term prophylaxis in hereditary angioedema have limitations.To assess the efficacy of lanadelumab, a fully human monoclonal antibody that selectively inhibits active plasma kallikrein, preventing attacks.Phase 3, randomized, double-blind, parallel-group, placebo-controlled trial conducted at 41 sites Canada, Europe, Jordan, and United States. Patients were randomized between March 2016, September 9, 2016; last day follow-up was April 13, 2017. Randomization 2:1...
Hereditary angioedema with C1 inhibitor deficiency is characterized by recurrent, unpredictable swelling episodes caused uncontrolled plasma kallikrein generation and excessive bradykinin release resulting from cleavage of high-molecular-weight kininogen. Lanadelumab (DX-2930) a new the potential for prophylactic treatment hereditary deficiency.We conducted phase 1b, multicenter, double-blind, placebo-controlled, multiple-ascending-dose trial. Patients were randomly assigned in 2:1 ratio to...
Hereditary angioedema (HAE) is a chronic disease with high burden of that poorly understood and often misdiagnosed.Availability treatments, including C1 esterase inhibitor (C1INH) replacement, ecallantide, icatibant, marks significant advance for HAE patients.We aimed to better understand the current state care, from patient perspective, after introduction several novel therapies.One session United States Angioedema Association 2013 summit was devoted data collection this study.Patients...
We conducted our first patient survey at the 2013 hereditary angioedema (HAE) summit and learned that, despite several novel therapies, burden of disease was high.To determine, from patient's perspective, if any improvements in current state HAE care occurred over a two-year period between summits.A 2015 Hereditary Angioedema Association conference by using paper surveys that aimed understanding care. Questions included characteristics, disease, satisfaction with treatment options....
Availability of effective treatment for acute attacks is expected to transform the care hereditary angioedema (HAE) patients. We felt that it would be interest test these assumptions by examining perceptions HAE patients regarding impact therapies have had on their lives. Patients at a United States Association summit meeting were asked rate burden currently and compare recall with 2009 when not available. Questions covered five domains: psychological/emotional status, ability carry out...
Hereditary angioedema (HAE) caused by C1-esterase inhibitor deficiency is an autosomal-dominant disease resulting from a mutation in the C1-inhibitor gene. HAE characterized recurrent attacks of intense, massive, localized subcutaneous edema involving extremities, genitalia, face, or trunk, submucosal upper airway bowels. These symptoms may be disabling, have dramatic impact on quality life, and can life-threatening when affecting airways. Because manifestations severity are highly variable...
Hereditary angioedema (HAE) caused by C1-esterase inhibitor deficiency is an autosomal-dominant disease resulting from a mutation in the C1-inhibitor gene. HAE characterized recurrent attacks of intense, massive, localized subcutaneous edema involving extremities, genitalia, face, or trunk, submucosal upper airway bowels. These symptoms may be disabling, have dramatic impact on quality life, and can life-threatening when affecting airways. Because manifestations severity are highly variable...
Hereditary angioedema (HAE) due to C1-inhibitor deficiency is a rare autosomal dominant disease that manifests as sudden unpredictable attacks of subcutaneous or submucosal edema affecting the skin, intestine, and upper airway. Ecallantide plasma kallikrein inhibitor indicated for treatment HAE in patients aged 16 years older. This analysis examines safety efficacy ecallantide <18 age.Data 9 17 treated subcutaneously with 30 mg placebo were pooled from 4 clinical studies (2 double-blind,...
Induction of tolerance protocols have been applied successfully to manage allergic reactions many medications. Hypersensitivity natalizumab (TYSABRI®) recognized as a growing problem. In circumstances where hypersensitivity reaction medication has occurred, but no suitable alternative exists, drug induction may be considered. Drug were performed in three patients with prior natalizumab. All tolerated the protocol without adverse reactions, allowing for safe reintroduction To conclude, this...